Traumatic brain injury, TBI, has been mentioned in the annual reports as a topic of research by ATH. This Chinese report below is an exceptional TBI report because if found that in TBI also heart can get problems because of iron overload caused by the injury. IMO, other traumas may have this kind of problem. Maybe ATH is aware of this problem but anyhow it seems important, especially when ATH has the medicine to treat this, I believe.

Highlights
•TBI causes ferroptosis in the heart tissue.
•TBI induces iron overload in the heat tissues
.•Iron overload is involved in ferroptosis in the heart and promotes TBI-induced cardiac inflammation via ROS/p38 MAPK/NFκB pathway.

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Biochem Biophys Res Commun

. 2023 Sep 28:682:46-55.

doi: 10.1016/j.bbrc.2023.09.088. Online ahead of print.

Iron overload enhances TBI-induced cardiac dysfunction by promoting ferroptosis and cardiac inflammation

Ruilong Peng ¹, Xilei Liu ², Cong Wang ¹, Fanjian Li ¹, Tuo Li ³, Lei Li ¹, Hejun Zhang ⁴, Yalong Gao ⁵, Xuefang Yu ⁶, Shu Zhang ⁷, Jianning Zhang ⁸

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• PMID: 37801989

DOI: 10.1016/j.bbrc.2023.09.088

Abstract

Previous studies have proved that cardiac dysfunction and myocardial damage can be found in TBI patients, but the underlying mechanisms of myocardial damage induced by TBI can't be illustrated. We want to investigate the function of ferroptosis in myocardial damage after TBI and determine if inhibiting iron overload might lessen myocardial injury after TBI due to the involvement of iron overload in the process of ferroptosis and inflammation. We detect the expression of ferroptosis-related proteins in cardiac tissue at different time points after TBI, indicating that TBI can cause ferroptosis in the heart in vivo. The echocardiography and myocardial enzymes results showed that ferroptosis can aggravate TBI-induced cardiac dysfunction. The result of DHE staining and 4-HNE expression showed that inhibition of ferroptosis can reduce ROS production and lipid peroxidation in myocardial tissue. In further experiments, DFO intervention was used to explore the effect of iron overload inhibition on myocardial ferroptosis after TBI, the production of ROS, expression of p38 MAPK and NF-κB was detected to explore the effect of iron overload on myocardial inflammation after TBI. The results above show that TBI can cause heart ferroptosis in vivo. Inhibition of iron overload can alleviate myocardial injury after TBI by reducing ferroptosis and inflammatory response induced by TBI.